HIV latency
HIV-1 can build up a condition of latent disease at the level of individual T cells. Inactively contaminated cells are uncommon in vivo and seem to emerge when enacted CD4+ T cells, the real targets cells for HIV-1, end up infected and survive sufficiently long to return to a resting memory state, which is nonpermissive for viral quality articulation. Since inert infection lives in memory T cells, it holds on inconclusively even in patients on powerful antiretroviral treatment. This latent reservoir is recognized as a major barrier to curing HIV-1 infection. The molecular mechanisms of latency are unpredictable and incorporate the absence in resting CD4+ T cells of nuclear forms of key host translation factors (e.g., NFκB and NFAT), the absence of Tat and related host factors that advance proficient transcriptional prolongation, epigenetic changes repressing HIV-1 quality articulation, and transcriptional impedance. These viruses are released from latently infected cells that have that have become activated and perhaps from other stable reservoirs but are blocked from additional rounds of replication by the drugs. Edelweiss Journal of AIDS journal is a Peer reviewed journal maintaining high standards of scientific excellence and its editorial board ensures a thorough review process.
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